Preventing Cisplatin-Induced Hearing Loss 

How can we prevent cisplatin-induced hearing loss? Cisplatin is a widely used chemotherapeutic agent, but its clinical use is often limited by irreversible hearing loss. Our research investigates the molecular and vascular mechanisms underlying cisplatin-induced cochlear injury, with a particular focus on blood–labyrinth barrier dysfunction in the stria vascularis. We found that co-treatment with carbon monoxide–releasing molecule-2 (CORM-2) alleviates ototoxicity by:

- reducing platinum accumulation

- suppressing inflammatory responses

- preserving vascular integrity

These findings suggest potential therapeutic strategies to protect the inner ear during cisplatin chemotherapy.

Macrophage Dynamics in Cochlear Injury and Repair 

How do immune cells shape cochlear injury and recovery? Our research focuses on the dynamic immune responses of macrophages in the cochlea during hearing loss. In response to acoustic stress and other insults, cochlear macrophages undergo changes in activation, morphology, and spatial distribution. We investigate the interactions between:

- CX3CR1⁺ resident macrophages

- CCR2⁺ infiltrating monocytes

particularly within key cochlear regions such as the stria vascularis and spiral ligament. By defining the spatiotemporal dynamics of cochlear immune cells, our goal is to understand how immune responses influence cochlear injury and recovery, and how they shape the outcome of noise-induced hearing loss, including temporary and permanent threshold shifts.

Systemic Inflammation and Cochlear Vulnerability 

Our research investigates how systemic metabolic disorders influence cochlear susceptibility to hearing loss. Emerging evidence suggests that metabolic diseases disrupt inner ear homeostasis through systemic inflammatory signaling, forming a functional liver–inner ear axis. We study how circulating inflammatory mediators derived from metabolic liver disease alter the cochlear microenvironment, including:

- vascular barrier integrity

- inflammatory responses

By defining how systemic inflammation primes the cochlea for injury, our goal is to understand why metabolic dysfunction increases susceptibility to noise-induced hearing loss and delayed auditory recovery.

Biomaterial-Based Drug Delivery for the Inner Ear 

Our research aims to develop advanced drug delivery systems for inner ear diseases, where therapeutic efficacy is limited by anatomical barriers and rapid drug clearance. We design injectable biomaterial-based platforms that enable sustained and targeted drug release to the cochlea. In particular, we develop:

- thermo-responsive hydrogels

- biodegradable delivery systems

for intratympanic administration to improve drug retention and therapeutic efficacy. By integrating biomaterials engineering with cochlear biology, our goal is to enhance local drug delivery, protect sensory hair cells, and promote recovery from noise-induced and inflammatory inner ear disorders.

Central Neural Mechanisms of Hearing Loss  

How does hearing loss alter brain function and neural circuits? Hearing loss is increasingly recognized as a complex brain disorder that extends beyond peripheral sensory damage to involve the central nervous system. Despite similar degrees of peripheral injury, patients exhibit diverse clinical outcomes, underscoring the role of central auditory and non-auditory brain regions. 

It induces widespread changes across brain networks, including:

- neural circuit reorganization

- increased cognitive load

- elevated risk of cognitive decline and dementia

However, the molecular and cellular mechanisms linking peripheral damage to central neural dysfunction remain largely unclear. To address this gap, our research aims to define these mechanisms and develop novel therapeutic strategies targeting brain circuits affected by hearing loss.